Decreased E‐cadherin expression is associated with increased susceptibility to infection in WB (rat liver epithelial) cells following infection with Herpes Simplex Virus‐ Type 2 (HSV‐2)

E‐cadherin expression is decreased in a permissive rat liver epithelial cell line (WB) compared to less permissive mutant cells. Previous research has shown that infection with herpes simplex virus‐type 2 (HSV‐2) attenuates gap junctional communication (GJIC) in WB cells long before visible signs of infection. In order to elucidate this mechanism, membrane proteins in gap junction communication‐deficient and –rescued mutant cell lines (WB‐aB1 and WB‐a32/10 cells), which are less permissive to HSV‐2 infection, were compared with the wild type (WB) cell line. Localization of gap junction protein connexin 43 (Cx‐43) and tight junction protein Zonula occludens‐1 (ZO‐1) was monitored using dual labeled immunofluorescence. Prior to infection, all three cell lines expressed Cx‐43 and ZO‐1 was present uniformly throughout the membrane. Following infection, the wild type WB cells demonstrated a change in localization of Cx‐43 and ZO‐1 into the cytoplasm, while the WB‐aB1 and WB‐a32/10 cells retained membrane localization that was similar to control, uninfected cells. Western analysis of these proteins showed little difference in protein content between the three cell lines, possibly indicating that they do not contribute to the decrease in susceptibility of the WB‐aB1 and WB‐a32/10 cells to HSV‐2 infection. In contrast, immunofluorescence and Western blot analysis demonstrated that the adherens junction protein, E‐cadherin, was found in higher amounts in the less permissive cell lines compared to the wild type cell line. These results suggest that the presence of E‐cadherin plays a role in the permissiveness to infection in the WB cells. Research was supported by NIH AREA grant to GM, RW, and MK.